Glucose transporters in the human placenta

Glucose transporters in the human placenta
复制标题

DOI:
10.1053/plac.1999.0448
复制
发表时间:
2000-01-01
期刊:
影响因子:
3.8
通讯作者:
Illsley, NP
Illsley, NP
中科院分区:
医学3区
文献类型:
--
作者:
Illsley, NP

文献摘要

被引文献

相似文献

针对易化扩散葡萄糖转运蛋白(GLUT)家族的各种成员的抗体和cDNA探针的可用性使研究人员能够更清楚地了解胎盘摄取和经胎盘转运葡萄糖的机制。本文综述了人类胎盘葡萄糖转运的研究,目的是提供一个模型,该模型描述了胎盘中存在的转运蛋白亚型,它们的细胞定位和功能意义。GLUT 1葡萄糖转运蛋白,存在于合胞体屏障的微绒毛膜和基底膜,是参与葡萄糖经胎盘运动的主要同种型。虽然GLUTS mRNA广泛分布,但GLUTS蛋白定位于血管内皮的动脉成分,在那里它可能在增强经胎盘葡萄糖转运中发挥作用。这一数据与其他哺乳动物物种(如小鼠、大鼠和绵羊)的情况相反,在其他哺乳动物物种中,GLUTS蛋白不仅存在于进行经胎盘转运的上皮细胞中,而且随着妊娠的进展成为日益突出的同种型。GLUT 1在人合体滋养层中的不对称分布(微绒毛>基底)意味着基底GLUT 1在经胎盘转移中充当限速步骤。因此,基础GLUT 1的变化有可能导致葡萄糖经胎盘转运的改变。虽然在胎儿宫内发育迟缓中合胞体GLUT 1表达似乎没有变化,但在糖尿病妊娠中观察到基础GLUT 1表达和活性增加,对母体-胎儿葡萄糖通量有显著影响。除了对高血糖和低血糖的影响外,对胎盘中葡萄糖转运蛋白的调节知之甚少。GLUT 1的表达和活性似乎与细胞外葡萄糖浓度呈负相关,然而在生理范围内,GLUT 1的表达相对不受葡萄糖浓度的影响。仍然需要有关妊娠发育、宫内生长迟缓明确条件下的表达和活动、糖尿病妊娠中观察到的变化的机制和后果以及葡萄糖以外的外部因素在调节胎盘葡萄糖转运中的作用的信息。(C)2000年哈考特出版社有限公司
The availability of antibodies and cDNA probes specific for the various members of the facilitated-diffusion glucose transporter (GLUT) family has enabled researchers to obtain a much clearer picture of the mechanisms for placental uptake and transplacental transport of glucose. This review examines studies of human placental glucose transport with the aim of providing a model which describes the transporter isoforms present in the placenta, their cellular localization and functional significance. The GLUT1 glucose transporter, present an both the microvillous and basal membranes of the syncytial barrier, is the primary isoform involved in the transplacental movement of glucose. Although GLUTS mRNA is widely distributed, GLUTS protein is localized to the arterial component of the vascular endothelium, where it may play a role in enhancing transplacental glucose transport. This data is in contrast to the situation in other mammalian species, such as the mouse, rat and sheep, where GLUTS protein is not only present in those epithelial cells which carry out transplacental transport but becomes an increasingly prominent isoform as gestation progresses. The asymmetric distribution of GLUT1 in the human syncytiotrophoblast (microvillous > basal) means that basal GLUT1 acts as the rate limiting step in transplacental transfer. Changes in baser GLUT1 therefore have the potential to cause alterations in transplacental transport of glucose. Although there appear to be no changes in syncytial GLUT1 expression in intrauterine growth retardation, in diabetic pregnancies increases in basal GLUT1 expression and activity have been observed, with significant consequences for the maternal-fetal flux of glucose. Little is known of glucose transporter regulation in the placenta save for the effects of hyper- and hypoglycemia. GLUT1 expression and activity appear to be inversely related to extracellular glucose concentration, however within the physiological range, GLUT1 expression is relatively refractory to glucose concentration. Information is still needed on gestational development, on the expression and activity in well-defined conditions of intrauterine growth retardation, on the mechanisms and consequences of the changes observed in diabetic pregnancy and on the role of external agents other than glucose in regulating placental glucose transport. (C) 2000 Harcourt Publishers Ltd.